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Curcumin [bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] was studied by means of UV–VIS absorption spectroscopy and nanosecond laser flash photolysis in 1,4-dioxane–water mixtures in a series of dioxane–water volume ratios. The transient characteristics were found to be dependent on the amount of water. In pure dioxane the triplet state of the molecule in its enolic form was detected (λmax = 720 nm, τ = 3.2 μs), whereas upon water addition, the diketo form was found to prevail, because of the perturbation of intramolecular H-bonded structure. This led to hydrogen abstraction from dioxane by curcumin triplet state and the formation of the corresponding ketyl radical (λmax = 490 nm, τ ∼ 10 μs). Laser flash photolysis measurements, carried out in solvents of different polarity and proticity (benzene, cyclohexane and various alcohols), allowed the transient assignments to be confirmed, supporting our interpretation.
The absorption and emission spectral properties of thioflavin T (TFT) in Nafion (Nf) and cellulose matrices have been studied. Formation of the emittive dimer is observed in both matrices. The monomer TFT emission is blueshifted in Nafion membrane (Nf), whereas it is redshifted in cellulose membrane when compared with the emission in aqueous solution. The dimer emission of TFT in the Na-Nf membrane undergoes off–on switching with acids and alkalis. The TFT molecule undergoes protonation in the H-Nf and the protonated dye is fluorescent. The dimer emission of TFT is not observed in the dry H-Nf membrane because of the protonation of the TFT molecule. The diffusion coefficient and the free energy of hydrophobic interaction for the TFT molecule in the Nf membrane are calculated. The TFT molecule experiences hydrophobic and electrostatic interactions in the Nf matrix, whereas it experiences a polar environment in the cellulose membrane. The 3D emission spectral studies support the formation of the emittive dimer in both Nf and cellulose matrices.
The azide ion is a strong physical quencher of singlet molecular oxygen (1O2) and is frequently employed to show involvement of 1O2 in oxidation processes. Rate constants (kq) for the quenching of 1O2 by azide are routinely used as standards to calculate kq values for quenching by other substrates. We have measured kq for azide in solvent mixtures containing deuterium oxide (D2O), acetonitrile (MeCN), 1,4-dioxane, ethanol (EtOH), propylene carbonate (PC), or ethylene carbonate (EC), mixtures commonly used for many experimental studies. The rate constants were calculated directly from 1O2 phosphorescence lifetimes observed after laser pulse excitation of rose bengal (RB), used to generate 1O2. In aqueous mixtures with MeCN and carbonates, the rate constant increased nonlinearly with increasing volume of organic solvent in the mixtures. kq was 4.78 × 108M−1 s−1 in D2O and increased to 26.7 × 108 and 27.7 × 108M−1 s−1 in 96% MeCN and 97.7% EC/PC, respectively. However, in EtOH/D2O mixtures, kq decreased with increasing alcohol concentration. This shows that a higher solvent polarity increases the quenching efficiency, which is unexpectedly decreased by the proticity of aqueous and alcohol solvent mixtures. The rate constant values increased with increasing temperature, yielding a quenching activation energy of 11.3 kJ mol−1 in D2O. Our results show that rate constants in most solvent mixtures cannot be derived reliably from kq values measured in pure solvents by using a simple additivity rule. We have measured the rate constants with high accuracy, and they may serve as a reliable reference to calculate unknown kq values.
Studies of the photoimmunoprotective properties of sunscreens have produced disparate results. In this study in hairless mice, we compared two UVB absorbers, 2-ethylhexyl-p-methoxycinnamate (2-EHMC) and octyl-N-dimethyl-p-aminobenzoate (o-PABA), individually formulated in a common base lotion with a sunburn protection factor of 6. We measured their capacity to protect against suppression of the contact hypersensitivity (CHS) induced by three daily exposures of the dorsum to 6× the minimal erythemal/edematous dose (MED) of solar-simulated UV radiation (SSUV), in comparison with base lotion–treated mice exposed to 3 × 1 MED of SSUV. All treatments produced a similar minimal erythema. CHS was equally suppressed in mice irradiated through o-PABA and base lotion, but the suppression was significantly reduced in mice irradiated through 2-EHMC. Neither UVB absorber inhibited the epidermal photoisomerization to the immunosuppressive mediator, cis-urocanic acid. However, when mice were treated with exogenous cis-urocanic acid topically on the dorsum, but not when injected subcutaneously on the abdomen, suppression of CHS was observed in o-PABA– and base lotion–treated mice, but not in 2-EHMC–treated mice. Thus, the enhanced immunoprotection in mice irradiated through 2-EHMC apparently resulted from the direct inactivation of epidermal cis-urocanic acid by 2-EHMC. We conclude that comparative assessment of photoimmunoprotection by UV absorbers requires SSUV, erythemally matched exposures and consideration of potential interactions with cutaneous molecules.
Ground-based measurements of solar UV spectral irradiance made from Ushuaia, Argentina at latitude 55°S reveal a large degree of variability among corresponding months of different years over the period from September 1990 through April 1998. The magnitude and wavelength dependence of year-to-year changes in monthly spectral UV-B irradiation are consistent with expectations based on the behavior of column ozone and cloudiness. When combined with satellite measurements of column ozone, a regression model fit to the ground-based data set allows estimates of monthly UV-B irradiation over a time frame of two decades, 1978–1998, during several months of the year. Results show a general increase in ground-level irradiation at 305.0 nm from the end of the 1970s to the early 1990s during calendar months from September through December. This is followed by generally smaller irradiances through the middle to late 1990s for all months except November, where the increase continues through the end of the data record. The long-term variability in monthly irradiation over the time period studied is more complicated than can be described by a simple linear trend.
Fourier transform–based spectroscopic imaging was used for direct, time-resolved, analysis of UV-irradiated anthracene crystallites. Well-resolved fluorescence spectra were obtained at a spatial resolution of 1 μm. The appearance of such photochemical by-products as dianthracene and anthraquinone was monitored throughout the irradiation experiments. Under deaerated conditions, photolysis of anthracene was accompanied by formation of dianthracene. When performed under aerated conditions, however, the spectral data indicated formation of both dianthracene and anthraquinone. Spectral features obtained for the directly monitored photolysis of anthracene are discussed in respect to the structural and compositional modifications in such crystallites. Capabilities of the spectral imaging device for the quantification of the photochemical products of anthracene are discussed.
The ultraviolet (UV) doses of American young adults were never measured, but are needed for assessing UV-related health risks. These doses were calculated using a novel approach. The National Human Activity Pattern Survey recorded the daily minute-by-minute activities of about 2000 young adults (0–19 years) over the course of 2 years to assess their exposure to environmental pollutants. From that survey, only the outdoor daylight data of northern and southern girls and boys were extracted and stratified by season and age to find the time American children (0–5 and 6–12 years) and adolescents (13–19 years) spend outside. They spend about 10% of the day outdoors, but only get about 30% of the available terrestrial UV radiation (on a horizontal plane). American children have about the same percent personal ambients as adults (3.1%), 2.8% for girls and 3.4% for boys. Adolescents have the lowest personal ambients (2.6%), 2.1% for girls and 3.1% for boys. To get their UV doses, their percent ambients are multiplied by the total available terrestrial UV. Excluding vacation, the erythemally weighted UV doses for American children are 25 kJ/m2/year, 23 for girls and 28 for boys. Adolescents get the lowest UV exposure of any group, 21 kJ/m2/year, 18 for girls and 24 for boys. Young adult northern girls get 18 kJ/m2/year and boys get 21 kJ/m2/year, whereas southern girls get 24 kJ/m2/year and boys get 31 kJ/m2/year. The youngest children (0–5 years) get slightly higher summer doses. Thus, we can now assess the UV-related health risks for American children and adolescents.
Spectra are presented from a single 3D microcrystal of bacteriorhodopsin (bR) cooled to 170 K under various illumination conditions. This set is necessary and sufficient to assign the relevant crystal reference spectra. A spectral decomposition of the difference spectrum obtained following the trapping protocol of Royant et al. (2000) (Nature406, 645–648) is given, confirming that the low temperature L-intermediate was the species that dominated the structural rearrangements previously reported. Smaller contributions from the K and M spectral intermediates are also quantified. Mechanistic insights derived from the X-ray structures of the early bR intermediates are discussed.
To determine whether ultraviolet B (UVB) irradiation leads to activation of HIV in human skin, we conducted prospective and controlled studies in two academic medical centers in Texas from July 1995 to April 1999. HIV-positive patients with UV-treatable skin diseases were enrolled at each center, 18 subjects at one and 16 at the other. In one center, specimens from lesional and nonlesional skin biopsies were taken before and after sham- or UVB-irradiation administered in vivo or in vitro. In the other center, UVB phototherapy was administered three times weekly and specimens from skin biopsies were taken before and after 2 weeks (six treatments). Cutaneous HIV load was assessed using reverse transcriptase-polymerase chain reaction and reverse transcriptase-polymerase chain reaction in situ hybridization. UVB irradiation led to a 6–10-fold increase in the number of HIV in skin. To ascertain a role for nuclear factor kappa B (NFκB) in UVB-inducible HIV activation, two types of blockers, NFκB oligonucleotide decoy and sodium salicylate, were tested; each inhibited UVB-inducible HIV activation in skin partially. We conclude that UVB irradiation leads to increased numbers of HIV in human skin via processes that include release of cytoplasmic NFκB.
Photodynamic therapy (PDT) treatment of both malignant and benign skin diseases has proven to be effective, and its use is increasing worldwide. However, preclinical studies using murine models have shown that PDT of the skin inhibits cell-mediated immune reactions, as measured by the suppression of the contact hypersensitivity (CHS) reaction. We have previously demonstrated that PDT enhances IL-10 expression in treated skin, and that the kinetics of induction of IL-10 is similar to the kinetics of suppression of systemic CHS reactions by cutaneous PDT. In the following report we have expanded upon these studies to demonstrate that cutaneous PDT, using Photofrin®, induces elevated levels of systemic IL-10 that persist for at least 28 days following treatment. The increase in systemic IL-10 correlates to a prolonged suppression of CHS of at least 28 days following cutaneous PDT. IL-10 has been implicated as the causative agent in the suppression of cell-mediated immune reactions by UVB and transdermal PDT. However, in the studies reported here we demonstrate that the suppression of CHS by cutaneous PDT occurs via an IL-10 independent mechanism, as administration of anti–IL-10 antibodies had no effect on the ability of PDT to induce CHS suppression. These results were further confirmed using IL-10 knockout (KO) mice. Cutaneous PDT of IL-10 KO mice resulted in CHS suppression that was not significantly different from suppression induced in wild-type mice. Thus, it appears as though IL-10 does not play a role in CHS suppression by cutaneous PDT. Suppression of cell-mediated immune reactions by UVB and transdermal PDT is reversible by IL-12, which is critical for the development of these reactions. We show that administration of exogenous IL-12 is also able to reverse CHS suppression induced by cutaneous PDT, suggesting that whereas suppression of cell-mediated immune reactions by UVB, transdermal PDT and cutaneous PDT occurs via different mechanisms, a common regulatory point exists.
In this study the endogenous fluorescence signal attributed to reduced nicotinamide adenine dinucleotide (NADH) has been measured in response to photodynamic therapy (PDT)–induced damage. Measurements on cells in vitro have shown that NADH fluorescence decreased relative to that of controls after treatment with a toxic dose of PDT, as measured within 30 min after treatment. Similarly, assays of cell viability indicated that mitochondrial function was reduced immediately after treatment in proportion to the dose delivered, and the proportion of this dose response did not degrade further over 24 h. Measurements in vivo were used to monitor the fluorescence emission spectrum and the excited state lifetime of NADH in PDT-treated tissue. The NADH signal was defined as the ratio of the integrated fluorescence intensity of the 450 ± 25 nm emission band relative to the fluorescence intensity integrated over the entire 400–600 nm range of collection. Measurements in murine muscle tissue indicated a 22% reduction in the fluorescence signal immediately after treatment with verteporfin-based PDT, using a dose of 2 mg/kg injected 15 min before a 48 J/cm2 light dose at 690 nm. Control animals without photosensitizer injection had no significant change in the fluorescence signal from laser irradiation at the same doses. This signal was monotonically correlated to the deposited dose used here and could provide a direct dosimetric measure of PDT-induced cellular death in the tissue being treated.
The skin of nude mice was exposed to erythemogenic doses of UV radiation, which resulted in erythema with edema. An ointment containing 5-aminolevulinic acid (ALA) was topically applied on mouse and human skin. Differences in the kinetics of protoporphyrin accumulation were investigated in normal and UV-exposed skin. At 24 and 48 h after UV exposure, skin produced significantly less protoporphyrin IX (PpIX) than skin unexposed to UV. Human skin on body sites frequently exposed to solar radiation (the lower arm) also produced less PpIX than skin exposed more rarely to the sun (the upper arm). It is concluded that UV radiation introduces persisting changes in the skin, relevant to its capability of producing PpIX from ALA. The observed differences in ALA-induced PpIX fluorescence may be the result of altered penetration of ALA through the stratum corneum or altered metabolizing ability of normal and UV-exposed skin (or both).
We report that exo- and endogenous guanosine 3′,5′-cyclic monophosphate (cGMP) specifically influenced the photophobic response. In behavioral experiments the slowly hydrolyzable and membrane-permeable analogs of cGMP (8-bromo-cGMP [Br-cGMP] and N6,2′-o-dibutyryl-cGMP) dramatically prolonged the time for ciliary stop response and decreased the duration of ciliary reversal in a dose-dependent manner. When analogs of adenosine 3′,5′-cyclic monophosphate (cAMP) (8-bromo-cAMP or N6,2′-o-dibutyryl-cAMP) were used, no essential effects were detected on the kinetics of the photophobic response. Both nonspecific cyclic nucleotide phosphodiesterase (PDE) activity inhibitors (3-isobutyl-1-methylxanthine [IBMX] and 1,3-dimethylxanthine [theophylline]) and the highly specific cGMP–PDE activity inhibitor 1,4-dihydro-5-[2-propoxyphenyl]-7H-1,2,3-triazolo[4,5-d]pyrimidine-7-one (zaprinast) mimicked the effects of cGMP analogs. Treatment of cells with an inhibitor of guanylate cyclase activity (6-anilino-5,8-quinolinedione [LY 83583]) exerted an effect opposite to that of cGMP analogs and PDE activity inhibitors. The positive physiological effect of LY 83583 was significantly diminished in ciliates that were treated simultaneously with Br-cGMP. In an assay of cell cyclic nucleotide content, the exposure of dark-adapted Stentor to light evoked a transient decrease in the basal level of intracellular cGMP. Alterations in internal cGMP levels were more distinct when the intensity of applied illumination was increased. In the presence of IBMX or theophylline the basal content of cGMP was markedly enhanced, and the photoinduced changes in cGMP level were less pronounced. In this paper the possible whole molecular mechanism by which the ciliary orientation in Stentor is controlled by light is presented.
Depending on the size and shape of their azulenic chromophores, azulenic bacteriorhodopsin (bR) pigment analogs can exist as either an initial pigment P1, a more red-shifted final pigment P2 or an equilibrium mixture of both. The absorption spectra of red-shifted bR analogs exhibit characteristic narrow-band shapes similar to charge fully delocalized cyanine-like dyes. Therefore, all such red-shifted pigments are believed to be highly delocalized, bond-equalized carbocations. We have determined structural requirements that facilitate their formation. To describe fully the red-shift potentials of these retinal analogs, we have introduced a new parameter—percent red-shift (PRS). A large PRS value not only reflects the extent of red-shift, but is also suggestive of extensive delocalization of the positive charge. Relevance of these findings in consideration of the possibility of forming stable O-intermediates is presented. The postulated resonance hybrid-like structures for different cations of the positively charged protonated Schiff base chromophores are in fact structurally distinct species, equilibrating in response to local perturbations within the supramolecular protein environment.